The function of the cardiovascular system is vital for survival. Through blood circulation, body tissues obtain necessary nutrients and oxygen, and discard waste substances. In the absence of circulation, cells begin to undergo irreversible changes that lead to death. The muscular contractions of the heart are the driving force behind circulation.
Each of the heart's contractions, or heartbeats, is triggered by electrical impulses. These electrical impulses are sent from the sinoatrial node (the heart's natural pacemaker), which is located at the top of the upper-right chamber of the heart or right atrium. From there, the electrical impulses travel through the upper chambers of the heart (atria) and to the atrioventricular (AV) node, where they are transmitted to the lower chambers of the heart ventricles via the “bundle branches.” Thus, the electrical impulses travel from the sinoatrial node to the ventricles, to trigger and regulate the heartbeat.
An arrhythmia is an abnormal heartbeat resulting from any change, deviation or malfunction in the heart's conduction system—the system through which normal electrical impulses travel through the heart. Under normal conditions, each of the heart's contractions, or heartbeats, is triggered by electrical impulses. These electrical impulses are sent from the sinoatrial node (the heart's natural pacemaker), which is located at the top of the upper-right chamber of the heart or right atrium. From there, the electrical impulses travel through the upper chambers of the heart (atria) and to the atrioventricular (AV) node, where they are transmitted to the lower chambers of the heart ventricles via the “bundle branches.” Thus, the electrical impulses travel from the sinoatrial node to the ventricles, to trigger and regulate the heartbeat.
When the electrical “circuits” of the heart do not operate optimally, an arrhythmia may result. An arrhythmia may result in unusually fast (tachycardia) or unusually slow (bradycardia) heartbeats. The cause of an arrhythmia may be related to a previous heart condition (e.g., previous damage from a heart attack) or to other factors (e.g., drugs, stress, not getting enough sleep). In the majority of cases, a skipped beat is not medically significant. The most serious arrhythmias, however, contribute to approximately 500,000 deaths in the United States each year according to the American Heart Association. Sudden cardiac death (“cardiac arrest”) is responsible for approximately one-half of all deaths due to heart disease, and is the number one cause of death in the US, according to the North American Society of Pacing and Electrophysiology.
Almost all clinically important tachyarrhythmias are the result of a propagating impulse that does not die out but continues to propagate and reactivate cardiac tissue (referred to as “reentry”). Such tachyarrhythmias include sinus node reentry, atrial fibrillation, atrial flutter, atrial tychycardia, AV nodal reentry tachycardia, AV reentry (Wolff-Parkinson-White syndrome or concealed accessory AV connection), ventricular tachycardia, and bundled branch reentrant tachycardia.
For reentry to occur, there must exist a substrate in the cardiac tissue capable of supporting reentry (the “reentry circuit”). The activation wave front must be able to circulate around a central area of block and encounter a unidirectional block such that it is forced to travel in one direction around the central block. (If the activation wave front is permitted to travel in both directions around the block, the wave fronts will collide and die out.) Of importance is the conductance speed of the circulating wave front. If the conductance speed is too fast, the circulating wave front will arrive at its point of origin before the tissue has repolarized sufficiently to become excitable again. Thus, at least one area of slow conductance is part of the reentry circuit for virtually all clinical reentrant rhythms. Eliminating the slow conductance elements of a reentry circuit destroys the circuit.
Atrial fibrillation (AF) is the most common type of sustained arrhythmia, affecting two million people each year in the United States alone. Both atrial fibrillation and atrial flutter increase the risk of stroke. According to the American Heart Association, they lead to over 54,000 deaths in the United States each year. The risk of developing atrial fibrillation increases dramatically with age. As a result, approximately 70 percent of patients with atrial fibrillation are between the ages of 65 and 85 years old. AF is a rapid, abnormal heart rhythm (arrhythmia) caused by faulty electrical signals from the upper chambers of the heart (atria). Electrical signals should normally be coming only from the sinoatrial node in a steady rhythm—about 60 to 100 beats per minute. A heart experiencing AF presents two heart rates—an atrial rate and a heart rate. With AF, the atrial rate is 300-400 beats per minute while the heart rate is 100-175 beats per minute. This heart rate is the result of the AV node blocking out most of the atrial impulses, and allowing only the fewer impulses to emerge to the ventricle.
Certain arrhythmias are related to specific electrical problems within the heart. AV nodal reentrant tachycardia is an arrhythmia caused by an extra conducting pathway within the AV node. This allows the heart's electrical activity to “short circuit” or recycle within the AV nodal region.
AV reentrant tachycardia results from an extra conducting pathway that allows the electrical impulse to “short circuit” and bypass the AV node altogether. In this mode, the extra “circuit” directly links the atria and ventricles. In most cases, this pathway can only conduct “backwards”—from ventricles to atria. This is called a “concealed accessory pathway” since it cannot be diagnosed from a regular electrocardiogram (EKG). These arrhythmias may be treated medically, but can also be cured by catheter ablation. Less often, the extra pathway conducts in the forward direction (from atrium to ventricle) and is evident on the EKG, in which case the condition is called the Wolff-Parkinson-White syndrome (WPW). WPW syndrome may result in extremely rapid heartbeats and could potentially result in death. Symptomatic WPW syndrome generally requires catheter ablation.
A quite different (and life threatening) condition is ventricular fibrillation. Ventricular fibrillation involves a quivering of the ventricles instead of the atria. Unlike AF, it is life threatening because it results in 350 beats per minute or higher. The heart cannot keep that rate up for more than a few minutes without treatment (e.g., with a defibrillator).
Under some conditions, arrhythmias may be transient. For example, a patient may be experiencing a particular period of stress, an illness, or a drug (legal or otherwise) reaction. In other cases, more invasive treatments are helpful. For a slow heartbeat (bradycardia), the most common treatment is an electronic (artificial) pacemaker. This device, which is implanted under the skin and permanently attached to the heart, delivers an electrical impulse when a slowing or irregularity of the heart rhythm is detected. For abnormally fast heartbeat rates, an implantable cardioverter defibrillator (ICD) may be implanted. An ICD monitors and, if necessary, corrects an abnormally fast heartbeat. These devices may be lifesaving for patients with ventricular fibrillation or ventricular tachycardia. Another procedure is an electrophysiology study with catheter ablation. This is a procedure in which catheters are introduced into the heart from blood vessels in the legs and/or neck and radio frequency energy is used to very carefully destroy (ablate) the abnormal areas of the heart that are creating the arrhythmias.
In cardiac muscle, the muscle fibers are interconnected in branching networks that spread in all directions through the heart. When any portion of this net is stimulated, a depolarization wave passes to all of its parts and the entire structure contracts as a unit. Before a muscle fiber can be stimulated to contract, its membrane must be polarized. A muscle fiber generally remains polarized until it is stimulated by some change in its environment. A membrane can be stimulated electrically, chemically, mechanically or by temperature change. The minimal stimulation strength needed to elicit a contraction is known as the threshold stimulus. The maximum stimulation amplitude that may be administered without eliciting a contraction is the maximum subthreshold amplitude.
Throughout much of the heart are clumps and strands of specialized cardiac muscle tissue. This tissue comprises the cardiac conduction system and serves to initiate and distribute depolarization waves throughout the myocardium. Any interference or block in cardiac impulse conduction may cause an arrhythmia or marked change in the rate or rhythm of the heart.
Biphasic—either cathodal or anodal—current may be used to stimulate the myocardium. However, until the work embodied in U.S. Pat. Nos. 5,871,506 and 6,141,586 for example, anodal current was thought not to be useful clinically. Cathodal current comprises electrical pulses of negative polarity. This type of current depolarizes the cell membrane by discharging the membrane capacitor, and directly reduces the membrane potential toward threshold level. Cathodal current, by directly reducing the resting membrane potential toward threshold has a one-half to one-third lower threshold current in late diastole than does anodal current. Anodal current comprises electrical pulses of positive polarity. Presently, virtually all artificial pacemaking is done using stimulating pulses of negative polarity although the utility of anodal pulse has been demonstrated.
The typical implantable cardioverter/defibrillator (ICD) delivers an initial electrical countershock within ten to twenty seconds of arrhythmia onset, thereby saving countless lives. Improved devices have antitachycardia pacing capabilities in addition to cardioverting/defibrillating functions. These ICDs are capable of different initial responses to one or more tachycardia as well as a programmable sequence of responses to a particular arrhythmia.
The output energy level is generally set by a physician in accordance with a patient's capture threshold, determined at the time of heart implantation. This threshold represents the minimum pacing energy required to reliably stimulate a patient's heart. However, due to trauma associated with the stimulation, scar tissue grows at the interface between the implanted cardiac pacer leads and the myocardium. This scar tissue boosts the patient's capture threshold. To insure reliable cardiac capture, the output energy level is thus generally set at a level which is a minimum of two times greater than the initially measured capture threshold. A drawback to such an approach is that the higher stimulation level causes more trauma to the cardiac tissue than would a lower level of stimulation, and hence promotes the formation of scar tissue, thereby boosting the capture threshold. The higher stimulation level also shortens battery life. This is not desirable, as a shorter battery life necessitates more frequent surgery to implant fresh batteries.
Another drawback is the potential for patient discomfort associated with this higher stimulation level. This is because the higher stimulation level can stimulate the phrenic or diaphragmatic plexus or cause intercostal muscle pacing. Lastly, the higher stimulation is less effective, due to entry block.
Improvements to pacing technology have resulted in an enhanced conduction of electrical pulses associated with resultant heartbeats for those arrhythmia victims who do not respond to ordinary pacing. For example U.S. Pat. No. 6,343,232 B1 entitled “Augmentation of Muscle Contractility by Biphasic Stimulation” was issued to Morton M. Mower, M.D. That invention described increasing electrical conduction and contractility by biphasic pacing comprising an initial anodal pulse followed by a cathodal pulse. This technique increased the speed of conduction of the resultant beats by almost 100% over that produced by conventional pacing stimuli. However, this technique did not result in reversion to a sinus rhythm for all victims of cardiac conduction disorder.
What would be truly useful is to provide alternative methods of stimulating the myocardium and to inhibit the conduction of certain spurious electrical impulses in the heart as a substitution for, or as an enhancement to, conventional pacing and pharmaceutical therapies and/or to use the alternative method in conjunction with conventional pacing and safe pharmaceuticals to provide yet another method for overcoming cardiac conduction problems.